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Methyl 3-chloroasterric acid exerted anti-neuroinflammatory and antidepressant effects through the downregulation of

Yifei Zhang1, Mingna Sun2, Zhonghong Zhang1

  • 1School of Pharmacy, Shandong Medical and Pharmaceutical University, Yantai 264003, Shandong, China.

International Immunopharmacology
|April 29, 2026
PubMed

Insights

Methyl 3-chloroasterric acid (MC) shows antidepressant effects by modulating neuroinflammation and microglial polarization. This compound targets the P2Y1 receptor, offering potential for treating depression and neuroinflammatory conditions.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Immunology

Background:

  • Depression is a neuropsychiatric disorder linked to neuroinflammation.
  • Microglial polarization imbalance is a key mechanism in neuroinflammation.
  • Methyl 3-chloroasterric acid (MC) is a marine-derived compound with unexplored biological activity.

Purpose of the Study:

  • To investigate the antidepressant effects of MC.
  • To explore MC's impact on microglial polarization, neuroprotection, and the blood-brain barrier.
  • To elucidate the molecular mechanisms underlying MC's action, focusing on the NF-κB pathway and P2Y1 receptor.

Main Methods:

  • Assessed antidepressant effects of MC in vivo.
  • Investigated MC's effects on microglial polarization and neuroprotection.
  • Utilized NF-κB signaling pathway analysis.
  • Examined P2Y1 receptor (P2Y1R) expression and function.
  • Employed P2Y1R knockout mice and P2Y1R inhibitors for mechanistic studies.

Main Results:

  • MC demonstrated significant antidepressant effects.
  • MC modulated microglial polarization, protected nerve cells, and preserved blood-brain barrier integrity.
  • MC inhibited NF-κB pathway activation and reduced P2Y1R expression.
  • MC's effects on microglial polarization and NF-κB were confirmed to be P2Y1R-mediated.

Conclusions:

  • MC is a potential therapeutic agent for anti-neuroinflammation and anti-depression.
  • P2Y1R plays a crucial role in MC's mechanism of action.
  • P2Y1R represents a potential therapeutic target for neuroinflammation and depression.
Keywords:
DepressionNF-κBNeuroinflammationP2Y1R

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